亲细胞非均质分子脂质抑制人脑胶质瘤U87细胞株增殖的实验研究

Proliferation inhibition of human brain glioma U87 cells by cytotropic heterogeneous molecular lipid

目的研究亲细胞非均质分子脂质(cytotropic heterogeneous molecular lipid,CHML)对人脑胶质瘤U87细胞增殖的影响及其可能的作用机制。方法不同浓度CHML不同作用时间处理U87细胞后,采用MTT比色法检测细胞活力,流式细胞术检测细胞周期和凋亡,Western印迹法检测细胞周期相关蛋白和凋亡相关蛋白的表达。结果 CHML作用于U87细胞后,细胞生长受到明显抑制。流式细胞术检测显示,CHML使G0/G1期细胞比例升高,S期和G2/M期细胞比例降低。Annexin V-PI法发现,用药24 h后,U87细胞凋亡比例随着CHM L的浓度升高而上升。Western印迹法检测显示,CHML引起U87细胞的周期相关蛋白Cyclin D1和CDK6表达降低,p21表达升高,凋亡相关蛋白Bax和Caspase 3表达增高,Bcl-2表达下降。结论 CHML可能通过诱导细胞凋亡和G1期细胞周期阻滞抑制U87细胞的增殖。

Objective To investigate the effect of cytotropic heterogeneous molecular lipid（CHML）on proliferation of human brain glioma U87 cells. Methods U87 cells were treated with different concentration of CHM L for various time. Cell viability was detected by M TTassay. Apoptosis and cell cycle were analyzed by flowcytometry,and the expression of cell-cycle and apoptotic proteins were examined by Western blotting. Results After treated with CHM L,the growth of U87 cells were markedly inhibited. Flow cytometric analysis showed that CHM L increased the number of cells in G0/ G1 and reduced the percentage of cells in S and G2/ M phase. Annexin V-PI method indicated that apoptosis rates of U87 cells rose with the increasingconcentration of CHM L after 24 hours of treatment. Western blottingdemonstrated that CHM L down-regulated the expression of Bcl-2,cyclin D1 and CDK6,and up-regulated the expression of p21,Bax,and Caspase 3. Conclusion CHM L can inhibit proliferation of U87 cells by inducingcell apoptosis and cell cycle arrest in G1 phase.